Drugs Flashcards
Semisodium Valproate (Depakote)
Used in mania in Bipolar disporder. Is an anticonvulsant. mood stabilizer, reduces seizures. Dissociates to valproate ion in GI, binds and inhibits GABA transaminase, also may block reuptake. may also work by suppressing repetitive neuronal firing through inhibition of voltage-sensitive sodium channels.
Folate antagonist, teratogenic.inhibits the DHFR protein. This enzyme is used to activate folic acid in the human body before it can enter the folate metabolism cycle.
750mg/day
Lithium
Used in mania of Bipolar. anticonvulsant, mood stabaliser. Blocks NMDA receptors, reducing Ca inflow into post synaptic neurons, reducing excitatory effects of glutamate. 1800mg/day
Lamotrigine/lamictal
Bipolar mania. Anticonvulsant mood stabilizer. Blocks Na and Ca channels. dec glutamate release.
Folic acid/THF
prevent neural tube defects. Folate is needed for production of new cells, DNA RNA synthesis and preventing changes to DNA. Crucial role in the closure of anterior and posterior neuropores. Its better to take naturally occuring folates - folinic acid and THF. to prevent first NTD take 400ug daily in first trimester. To prevent reacurrance 4-5mg perday.
NSAIDs
inhibit COX so inhibit prostaglandin production - anti inflam and antipyretic. Thromboxanes - antiplatlet. Anti inflam reduce pain. Increased risk of MI.
Ibruprofen
weak non selective COX inhibitor. 300 - 400mg 3/4 times daily. max 2.4g daily.
Paracetamol
COX inhibitor in CNS mainly COX 2, no anti inflam effects in peripheral tissues. can cause kidney damage and if take 10 to 15g, can cause hepatotoxicity. 0.5-1g every 4-6 hours, max 4g daily.
opioids co codamol and morphine
bind to opioid receptors, mainly u. inhibit adenylyl cyclase so reduce intracellular cAMP. open K channels causing hyperpolarisation. inhibit Ca opening, reduce neurotransmitter release. Prodrug.
Gabapentin
anticonvulsant used to treat neuropathic pain. Inc GABA synaptic conc, by acting as a calcium channel modifier. 300mg on day 1, twice on day 2, thirce on day 3.
Lidocaine
Local anasthetic. blocks Na, preventing AP.
amoxicillin
antibiotic, B lactam ring.
Thrombolysis/tPA(alteplase)
administered within 4.5 hours of stroke. Inactivates thrombin and ADP. tPA is a protease that cleaves plasminogen to form plasmin, which cleaves fibrin and other coagulants to degrade thrombi.
Anticoagulation long term
Warfarin and Heparin, inhibit function of coagulating factors in clot formation.
antiplatlet long term
aspirin/clopidegrol. Inhibit the function of platelets in clot formation. inhibit generation of thromboxane to have antithrombotic effect. Inhibit ADP receptor on platlets, prevents cross linking.
types of drugs for heamorrhagic stroke
anticonvulsants - reduce seizures. antihypertensive reduce BP. osmotic diuretics dec intercranial pressure.
Benzodiazepines (diazepam) in GAD
anticonvulsant. binds to a subunit on GABA a receptor causing the chanell to open and Cl- to influx hyperpolarising the cell, reducing anxiety. Also inc affinity of the receptor to GABA. shouldnt be used for longer than 2 weeks. GABAA receptors lacking a γ subunit are insensitive to benzodiazepines.
sertraline
SSRi. block seratonin reuptake transporter protein. inc conc in synaptic cleft.
venlafaxine
SNRI. blocks seratonin and noradren reuptake.
pregabalin
anticonvolsant treats neuropathic pain in GAD inc GABA synaptic conc.
methylprednisolone, prednisone.
Anti inflammatory in MS. Corticosteroid. avoid long term use. 1g/day for 3 days. 500mg/day for 5 days. Glucocorticoids bind intracellular receptors that then dimerise, migrate to the nucleus, and interact with DNA to modify gene transcription, inducing synthesis of some proteins and inhibiting synthesis of others.
Glucocorticoids dramatically reduce the manifestations of inflammation, inhibiting both the early and the late manifestations of inflammation. This is due to their profound effects on the concentration, distribution, and function of peripheral leukocytes & lymphocytes and to their suppressive effects on the inflammatory cytokines and chemokines and on other mediators of inflammation.
The anti-inflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins.